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Cancer Research Laboratory, Department of Molecular and Cell Biology, University of California, Berkeley, California
Requests for reprints: David H. Raulet, Department of Molecular and Cell Biology, University of California, Berkeley, 489 Life Science Addition, Berkeley, CA 94720-3200. Phone: 510-642-9521; Fax: 510-642-1443; E-mail: raulet{at}berkeley.edu.
Although there is considerable knowledge of how DNA damage triggers cell cycle arrest, DNA repair, and apoptosis, little was known about its potential role in immune responses. Recently, we showed that genotoxic stress and stalled DNA replication forks induce the expression of ligands for the NKG2D receptor found in natural killer cells and certain T cells, cell types that are able to attack tumor cells. Chronic activation of this response in tumor cells may contribute to immune recognition, but it also imposes a selection mechanism for immune escape and malignant progression. This unique arm of the DNA damage response may have implications for understanding therapeutic responses, many of which induce the DNA damage response, and for designing more effective regimens to treat cancer. (Cancer Res 2006; 66(8): 3959-62)
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